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Contributions of early adversity to pro-inflammatory phenotype in infancy: the buffer provided by attachment security
Jeffrey R Measelle1, Jennifer C Ablow1
1a Psychology , University of Oregon , Eugene , OR , USA.
Insights
Early life adversity, including familial stress and maternal depression, is linked to infant inflammation. Secure attachment may protect infants from these effects, suggesting early origins of lifelong health risks.
Area of Science:
- Developmental psychology
- Immunology
- Public health
Background:
- Early life adversity is linked to later systemic inflammation.
- Few studies explore early infancy inflammation origins and disease vulnerability.
- Understanding early inflammation is crucial for predicting lifelong health outcomes.
Purpose of the Study:
- Examine associations between multiple early adversities and infant inflammation.
- Investigate the buffering role of infant-maternal attachment security.
- Identify origins of pro-inflammatory responses in infancy.
Main Methods:
- Assessed socioeconomic status, familial stress, maternal depression, and attachment security.
- Measured salivary pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and C-reactive protein.
- Analyzed data from 49 infants at 17 months old.
Main Results:
- Familial stress, maternal depression, and attachment security directly correlated with infant inflammation.
- Attachment security moderated the impact of maternal depression on inflammation.
- Early adversity exposure is associated with infant pro-inflammatory markers.
Conclusions:
- Familial stress and maternal depression in infancy are linked to heightened inflammation.
- Infant attachment security plays a moderating role in adversity's immunologic impact.
- Early life adversity may establish a pro-inflammatory state with long-term health implications.
Abstract:
Adversity early in life is associated with systemic inflammation by adolescence and beyond. At present, few studies have investigated the associations between different forms of adversity and inflammation during infancy, making it difficult to specify the origins of disease vulnerability. This study examined the association between multiple forms of early adversity - socioeconomic status disadvantage, familial stress, maternal depression, and security of attachment - and individual differences in a composite measure of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and tumor necrosis factor-alpha) and the inflammatory protein C-reactive protein that were collected via saliva when (n = 49) children were 17 months old. In addition to gauging the direct effects of adversity, we also tested the hypothesis that infants' attachment relationship with their mother might buffer infants against the immunologic effects of early adversity. Results show that familial stress, maternal depression, and security of attachment were directly associated with infant salivary inflammation and that attachment status moderated the effect of maternal depression. The findings suggest that exposure to certain forms of adversity very early in life may engender a pro-inflammatory phenotype with possible life-long implications for health.
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